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Pharm 3 Module 2: GI > drugs to treat GERD, PUD, IBD and h.pylori > Flashcards

drugs to treat GERD, PUD, IBD and h.pylori Flashcards

1
Q

what are the different treatment options for GERD

A

lifestyle modifications
antacids
surface agents
H2receptor antagonists (H2RAs)
proton pump inhibitors (PPI)

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2
Q

what is the MOA of Antacids

A

neutralize acid (raise pH)

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3
Q

what are the uses of antacids

A

mild, intermittent heartburn or reflux (<1 episode/week)

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4
Q

what is the PK of antacids

A

onset: 5 min
duration: 30-60 minutes

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5
Q

what are the types of Antacids

A

calcium hydroxide (tums, maalox)
aluminum hydroxide (mylanta, gaviscon)
magnesium hydroxide (mylanta, gaviscon)

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6
Q

what are the SE of calcium hydroxide antacids

A

constipation
hypercalcemia
alkalosis
acute or chronic renal injury

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7
Q

what are the SE of aluminum hydroxide antacids

A

constipation
hypophosphatemia
*caustion with renal failure

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8
Q

what are SE of magneisum hydroxide antacids

A

diarrhea,
hypermagnesemia
*caution with renal failure

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9
Q

what is the MOA of surface agents

A

coats esophageal/gastric mucosa, creates physical barrier between mucosa and acid

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10
Q

what are the uses of surface agents

A

short-term management of GERD symptoms (4-8 weeks for duodenal ulcer)
swallow after meals, avoid drinking/eating afterwards

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11
Q

what is the PK of surface agents

A

onset: 5 minutes
duration: 30-60 minutes

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12
Q

what are the types of surface agents

A

sucralfate
sodium alginate
bismuth

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13
Q

what are the SE of sucralfate

A

constipation
aluminum toxicity
*caution with: renal failure, DM

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14
Q

What is the MOA of H2RAs

A

blocks stimulation of gastric parietal cells by competing with histamine H2 receptor

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15
Q

what are the uses of H2RAs

A

GERD, dyspepsia, PUD
-less effective than PPI, may be useful as adjunct
-not effective for H/pylori

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16
Q

what is the PK of H2RAs

A

onset: 2 hours
Duration: 4-10 hours

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17
Q

what are H2RA durgs

A

cimetidine, famotidine

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18
Q

what are the SE of H2RAs

A

HA, dizziness, diarrhea, constipation
cimetidine: gynecomastia
prolonged use(>2yrs) may lead to B12 deficiency

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19
Q

what is the MOA of PPIs

A

block gastric H/K-ATPase, inhibiting gastric acid secretion

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20
Q

what is the uses of PPIs

A

GERD, dyspepsia, PUD, H.pylori
-most effective acid suppressing med

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21
Q

what is the PK of PPIs

A

onset: 1 hour
duration: ~24 hours
admin: 30-60 min before first meal of the day

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22
Q

what are the PPI medications

A

Omeprazole
Pantroprazole
Lansoprazole
Esomeprazole

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23
Q

what are the risks of PPIs

A

available for >25 yo. may double blinded RCTs over years have not supported initial safety concerns
longer term: malabsorption of some minerals and vitamins, increased risk of some diarrheal illnesses, bacterial pneumonia, acute interstitial nephritis (AIN), CKD, gastric polyps

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24
Q

what are the SE of PPIs

A

HA
nausea
abdominal pain
diarrhea

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25
what are drug interactions with PPIs
decreased absorption of certain HIV protease inhibitors increased concentration of digoxin, carbamazepine, theophylline; warfarin, diazepam, phenytoin Increased MTX concentration/toxicity decrease anti-platelet effect of Plavix decrease absorption of PO iron
26
what is the Tx of PUD
avoid offending agents anti-seretory agent (PPI) = mainstay of tx test for and treat h.pylori if present
27
what is the tx regimen for H/pylori
2 week duration Triple therapy: Clarithromycin + amoxicillin + PPI Quadruple therapy: bismuth subsalicylate + tetracycline + metronidazole + PPI
28
what is the MOA for Busmuth
stimulates prostaglandin/mucous/bicarb production in the stomach mild antimicrobial activity, specifically against H.pylori reduces inflammation
29
what is the SE of bismuth subsalicylate
black stools, black tongue (reversible) bismuth neurotocixity: encephalopathy, asepctic meningitis, seizures
30
what needs to be cautioned with bismuth use
other salicylates/ASA/NSAIDs increased risk of bleeding neurotoxicity tinnitus
31
what is the MOA of Misoprostol
synthetic prostaglandin E1 analog. Prostaglandins inhibit acid secretion by reducing the ability of parietal cells to respond to histamine
32
what is the use of Misoprostol
prevention of NSAID-induced gastric ulcers
33
what is the PK of Misoprostol
onset: 30 min duration: 3 hours
34
what are the SE of misoprotol
diarrhea abd pain HA avoid with magnesium containing antacids
35
what are the contraindications with misoprotol
caution: can induce uterine contractions BBW: contraindicated in pregnancy or women of childbearing age. may cause birth defects, premature birth, abortion, uterine rupture
36
what are the Prokinetic agents
Metoclopramide, doperidone, erythromycin
37
what is the MOA of Metoclopramide
dopamine antagonist (primarily). enhances upper GI tract response to Ach to enhance motility; increases colon motility and shortens transit time
38
what is the use of Metocloramide
gastroparesis, peristent GERD, N/V can be useful for diabetic patients short term use only given risk of TD: <12 weeks
39
what is the PK of Metoclopramide
onset: 30-60 min duration: 1-2 hours
40
what are the SE of metoclopramide
drowsiness dystonia HA
41
what are the contraindications with metoclopramide
BBW: can cause tardive dyskinesia (irreversible) CI: Gi hemorrhage, mechanical obstruction, perforation
42
what is the MOA of Domperidone
peripheral dopamine antagonist (does not cross BBB). increase esophageal peristalsis, gastric motility and gastric emptying; decreases small bowel transit time
43
what is the use of Domperidone
gastroparesis/motility disorders, N/V -not available in US
44
what are the SE of Domperidone
HA, migraines, xerostomia may increase prolactin levels -galactorrhea, gynecomastia
45
what is the MOA of erythromycin
macrolide antibiotic. Motilin agonist - increases gastric contractions (prokinetic)
46
what is the use of Erythromycin
gastroparesis (primarily used as antibiotic) used for max 4 weeks duration d/t tachyphylaxis
47
what are the SE of erythromycin
cardiovascular arrhythmias, QTc prolongation superinfection (C.diff) major inhibitor of CYP3A4 myasthenia gravis - may exacerbate or cause symptoms
48
what is the MOA of Neostigmine
acetylcholinesterase inhibitor
49
what is the use of Neostigmine
acute colonic pseudo-obstruction (primarily used for M. gravis, also post-op bladder distention/urinary retention)
50
what are the SE of neostigmne
Cardiac arrhythmias - especially bradycardia dizziness, drowsiness, diarrhea *caution with CVD
51
what are the treatment options for IBD
flares: glucocorticoids, aminosalicylates(5-ASAs) maintenacne: biologics, immunomodulatiors, aminosalicylates
52
what is the MOA of 5-ASAs
work topically on affected/inflamed areas of mucosa; anti-inflammatory and immunosuppresive activity
53
what is sulfasalazine and Mesalamine
aminosalicylate (5-ASA)
54
what is the use of 5-ASAs
generally used for mild-moderate UC (flares and maintenace) - can be used for mild colonic Crohn's disease (distal)
55
what are the SE of Sulfasalzine
Nausea HA rash arthralgia bone marrow suppression oligospermia in men (infertility) - reversible
56
what are the SE of Mesalamine
nausea HA diarrhea abdominal pain nephrotoxicity/interstitial nephritis - rare
57
what are the drug interactions iwth mesalamine
antacids, H2RAs, PPIs can diminish efficacy of mesalamine
58
what is the use of immunosuppresants
induce and maintain remission in both UC and Crohn's. good for pts who can not maintain remission when steroids are tapered down/off, can help reduce steroid dose -slow acting drug. can take ~3-6 montsh to observe effect
59
what are the immunosuppresant medicatiosn
Azathioprine, methotrexate, Adalimumab/ Infliximab
60
what is the SE of Azathioprine
N/V bone marrow suppression (anemia, leukopenia, thrombocytopenia) liver toxicity
61
what medications should be avoided with azathioprine
avoid with allopurinol (gout med) - leukopenia
62
what is the MOA of methotrexate
immunosuppressant, anti-inflammatory for IBD one of first antineoplastic drug developed. acts as folate antagonist, inhibiting DNA syntheses, repair and cellular replication
63
what is the USE of methotrexate
induce and maintain remission of Crohn's disease (less commonly used for UC)
64
what are the SE of methotrexate
diarrea n/v alopecia bone marrow suppression mucositis severe possibly fatal skin reactions, SJS, TEN
65
what are BBW with methotrexate
severe toxic/fatal SE hepatotoxicity potentially fatal opporunisitic infections lung disease teratogen
66
what is the MOA of biologics
bind and sequester TNF to decrease inflammatory response
67
what is the use of biologics
maintenance for moderate to severe IBD (mostly for Crohns disease. infliximab also used for UC)
68
what are the biologic medications
Adalimumab/ Infliximab
69
what is the SE of infliximab
injection site reaction/infusion reaction HA, abdominal pain, liver toxicity, heart failure, infections, URI risk of infection worse with concomitant immunosuppression no live vaccines while on therapy
70
what is the MOA of glucocorticoids
inhibits production of inflammatory cytokines and inhibit migration of inflammatory cells to affected area
71
what is the use of glucocorticoids
moderate-severe Crohn's and UC; helpful in early tx and during flares
72
what are the common glucocorticoids we use with IBD
PO: prednisone/prednisolone : Budesonide/entocort Rectal: hydrocortisone

Pharm 3 Module 2: GI (4 decks)

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